MTHFR Mutations First we’ll look at a few of your MTHFR mutations. According to research, these mutations are important and can be implicated in various disease states.

You have homozygous (red) mutation(s). These are the worst type of mutations. They include:

MTHFR A1298C MTHFR A1298C MTHFR A1298C is involved in converting 5-methylfolate (5MTHF) to tetrahydrofolate (THF). Unlike MTHFR C677T, the A1298C mutation does not lead to elevated homocysteine levels. This reaction helps generate BH4. BH4 is important for the detoxification of ammonia. The gene is compromised about 70% in MTHFR A1298C (+/+) individuals, and about 30% in people with a heterozygous (+/-) mutation.

BH4 acts as a rate limiting factor for the production of neurotransmitters and catecholamines including serotonin, melatonin, dopamine, norepinephrine, and epinephrine. A MTHFR A1298C + status may cause a decrease in any of these neurotransmitters or catecholamines. BH4 is also a cofactor in the production of nitric oxide. A dysfunctional BH4 enzyme may lead to mental/emotional and/or physical symptoms. Mercury, lead, and aluminum may act as a drain on Bh4

impossible, when you do respond, i also ran my data through mthfrsupport.com and got a longer report. I have a link to it which I’d like to send to you if you have an email. I don’t want to publicly post it since it has my name on it.

yisucks- Im working on yours, but im still feeling pretty ill and even when im feelin a little better my head is in quite a daze, so its takin some time. Yours is actually a little complicated and I want to give you a good report so its takin some time. Shoot me a pm at curezone, my name is the same over there.

Yours is pretty simple. You are the perfect example as to why a person should get a test done before they supplement methyl substances.

You dont have any noteworthy holdups in either your folate or methionine cycles, congratulations. You have mutations that are noteworthy, however, in another way. Your body is quite lethargic when it comes to breaking down dopamine and norepinephrine. The body “deactivates” them by attaching a methyl group to them. Because of this downregulation of useage of methyl groups, it would be incredibly easy for you to have too many methyl groups in your body. For this reason, you should stay away from not just methyl forms of vitamins, but it would probably be a good idea for you to stay away from methyl donors in general, you run the risk of becoming “overmethylated” very easily. You can find lists online. A hetero 1298 mutation isnt a huge deal, made even less problematic by your comt mutations. Low 1298= low bh4. Bh4 is required to make some neurotransmitters, since your not breaking dopamine down, your also not using up as much bh4 to make it. You might want to look up dopamine precursors, even dietary, and see if avoiding them helps you feel better if it is a problem for you. Tics, panic disorder, and bipolar disorder can all be related to too much dopamine, among other things im sure.

Your cbs 699 mutation could be causing you some problems, which would become worse if you started spinning the cycle faster with supplementation. That is actually an upregulation that basically results in the body making too many sulfur compounds, even toxic ones, and ammonia. This can have quite profound negative effects in some people, particularly those that are homozygotes. Treatment basically consists of minimizing or not eating sulfur compounds and if necessary supplementing with small amounts of molybdenum which the body needs to convert toxic sulfites into non toxic sulfates, and yucca root, which mops up ammonia.

Here is what heartfixer says about it:

CBS initiates the trans-sulfuration pathway, converting homocysteine in to cystathionine and its downstream metabolites. This is the most important Methyl Cycle defect and is present in 90% of the patients who we have tested. The CBS defect is an up regulation. CBS is operating at up to ten times its normal rate. Homocysteine and all of the upstream methyl cycle precursors will be “pulled down the CBS drain” to produce toxic levels of cystathionine metabolites. The C699T and (to a somewhat lesser extent) A360A defects are associated with CBS up regulation. Homozygotes (+/+) will be more severely affected than will be individuals heterozygous (+/-) for a CBS abnormality. We treat CBS ( +) individuals with dietary animal protein and sulfate restriction and supplements designed to neutralize ammonia and speed up clearance of sulfite/sulfate. Laboratory findings consist of an elevated urine sulfate level, a low or low normal blood homocysteine level, an elevated or high normal blood ammonia level, and positive findings of ammonia, sulfite, or sulfite upon Asyra testing. My initial observation is that individuals with high heavy metal burdens upon provocative challenge testing are likely to be CBS positive. CBS (+) individuals will be intolerant to sulfur containing drugs, nutritionals, and foodstuffs (I am +/- for CBS A360A and cannot tolerate DMPS or glucosamine sulfate. A cold beer tastes great but I do not like wine, which is high in sulfite).

Biochemistry – The 10-fold up regulation in CBS generates sulfur breakdown products (sulfite and sulfate, which stimulate the stress/cortisol “fight or flight” response), excess ammonia (in the process wasting BH4 which is used up detoxifying ammonia), hydrogen sulfide (producing “brain fog”), and alpha-keto glutarate (leading to “excitotoxicity”). The G6PDH enzyme system may be affected, leading to abnormalities in sugar control. Methylation intermediates will “fall through this drain”, so the entire system suffers; our defenses against viral invasion and toxicity suffer. Co-Q10 and Carnitine generation will fall off due to impaired methylation, and ATP levels fall, robbing you of energy.

Ammonia is produced during the metabolism of dietary protein. The CBS up regulation drains methyl cycle intermediates in to ammonia, more ammonia than your system can handle. Ammonia detoxification is metabolically expense, using up two molecules of BH4 per molecule of ammonia. BH4 is necessary to generate neurotransmitters (dopamine, serotonin, and norepinephrine) and nitric oxide, our key vasoprotective molecule. Thus it is easy to see how a CBS up regulation, by generating ammonia and depleting BH4, can set you up for neurological, psychological, and cardiovascular disease states. We cannot change your DNA. We cannot stop CBS from generating excess ammonia, but if we restrict animal protein in your diet, we can decrease your ammonia burden, preserving BH4, such that you can start making neurotransmitters and nitric oxide again – in other words, we can compensate for your genetic challenge. The herb Yucca, Dr. Yasko’s Ammonia support RNA product, and supplementation with charcoal and carnitine will bind up or neutralize ammonia, and add to your dietary efforts.

Sulfite is neurotoxic. Sulfite will be over produced by the CBS up regulation, and then requires conversion in to the less toxic sulfate molecule by the enzyme Sulfite Oxidase (SUOX). SUOX can easily be overwhelmed. Molybdenum is required for SUOX function, and is typically depleted in CBS (+/+) or (+/-) individuals. Molybdenum supplementation (3 drops or 75 mcg of e-lyte Molybdenum twice a day), Boron 3 mg/day, Vitamin E succinate 400 IU/day, and hydroxy-B12 2000 mcg/day are also utilized to speed up SUOX activity.

While sulfate is less toxic than is sulfite, it will stimulate the adrenergic (fight or flight) limb of the autonomic nervous system and stimulate a cortisol stress response, revving you up into an unrelenting biochemical overdrive. If you have a CBS defect, we need to restrict your sulfur intake, at least until your urine sulfate (and your body sulfate burden) has decreased. The amino acids methionine, taurine, and cysteine all contain sulfur; they are concentrated in animal protein (thus the restriction on animal protein intake). Many nutritional supplements (MSM, N-acetyl cysteine, glutathione) that are good for most people are a problem for you. While certain aspects of your health will benefit from these agents, they will add to your sulfate/sulfite overload problem, adversely affecting the Methyl Cycle Defect that is the common denominator to all of your health problems. Many drugs are loaded with sulfur (sulfates, sulfites, metabolically active sulfur), so if you are CBS positive and I treat your hypertension with the diuretic hydrochlorothiazide, your diabetes with the sulfonylurea drug glipizide, and your urinary tract infection with a sulfa containing antibiotic, I will be lowering your blood pressure, lowering your blood sugar, and clearing bacteria from your bladder, but I will also be adding to your sulfate burden, compromising your biochemistry, and contributing to an ongoing decline in your health. I will be treating the manifestations of an underlying problem and at the same time adding to the underlying problem. If I treat your Mercury overload with DMSA or DMPS, I will remove a toxin from your body, but if you are CBS (+), I will be adding to your sulfate/sulfite pool, and sulfate/sulfite overload due to the CBS up regulation is likely playing a key role in your sensitivity to heavy metals and/or your inability to clear them. We can avoid this. We can hold sulfur containing agents until your sulfate burden has come under control. Learn all you can about the sulfur content of foodstuffs, supplements, and prescription drugs. Sulfites and Chronic Disease by Rick Williams (available at the office or at http://www.readingtarget.com/nosulfites) is an invaluable resource. Do not expect us to know the sulfur content of foodstuffs. Some tips on low sulfur eating are included at the end of this document, but do not expect us to tell you what to eat. We can’t do this. We do not have this knowledge. Please attend our monthly Methyl Cycle support groups meetings, and you may sign up for individual (or group) dietary change counseling. It is your responsibility to become expert in this area. I will work with you to phase out high-sulfur drugs and nutritionals from your program, but don’t expect me to get in right every time – please study your food, drug, and supplement labels.

Excitotoxicity – The CBS up regulation leads to excess production of alpha-ketoglutarate, which is converted in to glutamate, a stimulatory neurotransmitter. Under normal circumstances, glutamate will be converted in to GABA, a calming neurotransmitter, but the enzyme systems that convert glutamate in to GABA are compromised by lead and mercury, the clearance of which seems to be compromised in individuals with methyl cycle defects (here is a situation where dysfunction of a genetically abnormal enzyme leads to acquired dysfunction of a genetically normal enzyme system). The result is “excitotoxicity”, stimulatory behavior in autistic kids (“stims”) and anxiety and sleeplessness in adults. We approach this problem by limiting alpha-ketoglutarate and glutamate rich foods from your diet (more on Excitotoxicity to follow; diet tips in appendix) and by supplementing you with GABA, aiming to restore GABA:Glutamate balance. GABA is initiated at 500 mg once or twice a day, advancing the dose as you see fit by your response.

The VDR (Vitamin D Receptor) Fok defect affects blood sugar control and pancreatic function. It does not affect dopamine metabolism. Dr. Yasko recommends Vitamin K and generalized support of pancreatic function and sugar regulation (low carbohydrate diet, supplementation with chromium, etc.) when the VDR Fok abnormality is an issue.

Methylation is only one chapter of the book, you should get the other panels too.

Just out of curiosity, have you ever had symptoms that would relate to the slowed breakdown of those neurotransmitters and if so what were/are they?

Impossible, where can I read more about this again? A book, internet? I would like to know because I think it would be beneficial for me, since I like to take a b vitamin. However, I would like to get it in the right proportions. You have probably posted before where to find it.

Your mutations are likely having a large influence on your health. You have some important snp’s, a few not even related to “undermethylation”. Some balance each other out fairly well. However, the deck is stacked against you in regards to b12, and you do have enough going on to slow down the cycle a bit. Keep in mind that just because you have some of these genes does not necessarily mean you are expressing them which is why physiological tests and trial and error with supplementation is so important. There is no great test for functional b12 status though, and considering your mutations and symptoms, I kind of take that as a given in your case.

Downregulations in these enzymes result in slowed breakdown of dopamine and serotonin. Vitamin D Receptor (VDR) Taq directly does not, but vitamin d status influences the creation of dopamine too, which influences methyl tolerance. The body makes these neurotransmitters inactive by attaching methyl groups to them. If you’re not using up methyl groups to do this, its easy to “overmethylate”, which has some rather unpleasant effects. Your deficit of bh4 due to your mthfr 1298 mutation somewhat offsets this, they help offset each really, and I would assume is enough to keep you from overproducing those particular neurotransmitters. Nonetheless, you should stay away from precursors and things like ssri’s. BH4 has other jobs too. A lack of it can impair b12 transport, contribute to pku (phenylalanine intolerance due to impaired ability to process it in the liver) that in lifelong cases usually shows with learning disabilities and a shy or withdrawn personality (though the 1298 mutation is not likely going to cause this directly, it can majorly contribute if other genetic abnormalities are present), and impair creation of nitric oxide. The recommendation is usually to supplement methylfolate actually, but you are probably much better off using up your (possible) limited tolerance of methyl groups taking mb12.

From heartfixer on BH4 and NOS:

In a BH4 dependent reaction, Nitric Oxide Synthase (NOS) converts Arginine in to Nitric Oxide, the molecule that resists plaque formation, vasospasm, and abnormal clotting. If you can make and maintain Nitric Oxide then you will not develop cardiovascular disease. If you have cardiovascular disease and if we can successfully reboot your Nitric Oxide system, than we can stabilize your disease. Every maneuver in drug and non-drug cardiovascular medicine that improves patient symptomatic status and outcome works on this system. Every risk factor (or causative factor for cardiovascular disease) compromises Nitric Oxide generation or maintenance. NOS is also involved in ammonia detoxification, a job that distracts it from its Nitric Oxide generating duties and which uses up BH4. Without adequate levels of BH4 Nitric Oxide Synthase will not convert Arginine in to beneficial Nitric Oxide, but rather in to undesirable free radical species such as superoxide or peroxynitrite.

From Pathways to Recovery:

The BH4 Three-Legged Stool

The added ammonia that is generated due to the enhanced breakdown of methylation cycle intermediates will also burden the adjoining urea cycle, thereby depleting a key intermediate called BH4, which plays a critical role in regulating neurotransmitters and therefore mood. BH4 is needed for serotonin, dopamine, conversion of phenylalanine to tyrosine and language-related function. The A1298C mutation in the MTHFR gene may also impact levels of BH4.

The drawing of a three-legged stool can help you visualize how the body maintains adequate levels of BH4. One leg is for CBS upregulations. The second leg is for MTHFR A1298C, another key SNP on the methylation pathway, which you will learn more about later in this chapter. The third leg is chronic bacteria/ aluminum. Stable BH4 levels require all three legs.

CBS upregulations weaken one leg of the stool by using up BH4 faster than it can be supplied. The NOS mutation can also exacerbate the CBS ammonia problem. In the adjacent urea cycle, inefficient NOS activity can lead to elevated ammonia levels, further draining BH4 limited stores. Reciprocally, CBS upregulations strain the urea cycle, where BH4 is needed to form nitric oxide. The formation of nitric oxide requires two BH4 molecules. With insufficient BH4, the body will instead produce peroxy nitrite (with one BH4 molecule), or super oxide (if no BH4 is available.) These two products can cause oxidative damage. The combination of CBS + and these other SNPs will further weaken this leg of the BH4 stool. MTHFR A1298C mutations (if present) impair the second leg by disrupting the recycling and regeneration of BH4. Chronic bacterial infection (which can lead to aluminum retention) weakens the third leg of the stool, because aluminum inhibits a key enzyme that helps to synthesize BH4. On this program, you will ultimately address all three legs of the BH4 stool by supporting the body to address chronic bacteria/aluminum, supporting the MTHFR A1298C mutation, and addressing CBS/ammonia issues. Other Interfaces that Impact BH4

Other mutations can also improve (or worsen) our BH4 stool’s sturdiness. While BH4 helps in the formation of neurotransmitters, other factors contribute to neurotransmitter breakdown. Bacterial infections trigger a more rapid breakdown of tryptophan (needed for serotonin). Low levels of BH4 have been associated with hypertension and arteriosclerosis, as well as with more severe parasitic infections. Parasitic infections also deplete B12 levels, impacting methylation cycle function.

Lack of BH4 may result in mast cell degranulation and lead to higher histamine levels, which can produce symptoms such as red ears and other hypersensitivity reactions. Serotonin synthesis as well as ammonia detoxification also require BH4. Elevated ammonia levels can cause flapping and other over-stimulatory behaviors.

Factors that lead to more ammonia, such as high protein diets, generate more ammonia that needs to be detoxified. Each molecule of ammonia requires two molecules of BH4 for ideal detoxification. Excess ammonia in the gut may alter the pH and aggravate imbalances in microbial flora. It’s obvious how these factors interact to impact ammonia detoxification as well as optimal BH4 levels for neurotransmitter synthesis. Keeping the ammonia levels under control is of paramount importance for overall health and wellness, especially for those with an MTHFR A1298C mutation, as any excess ammonia generated can drain stores of BH4. This can affect serotonin levels and to a certain extent cause fluctuations in dopamine (which translates into mood swings). Helping to restore adequate levels of BH4 should also aid in serotonin synthesis, maintaining dopamine levels as well as ammonia detoxification in a more stable manner.

This is the B12 triple whammy, which is not only a holdup of the methylation cycle but can also result in symptoms of low functional B12, such as neuropathy and myelination problems. MTRR is the enzyme that methylates cobalamin(b12) and you have a homozygous mutation of the gene that is known to have a major downregulatory effect on its performance. This results in less mb12 which slows the methylation cycle. MTR is the enzyme that transfers the methyl group from cobalamin to homocysteine and this mutation is an upregulation. This takes the already too little amount of mb12 you have and uses it up too quickly, leaving you with even less. This is important because mb12 is necessary for other functions in the body. ACAT may also result in a depletion of B12 as well.

You need to supplement with mb12, but theres a problem with that. You are not going to tolerate methyl donors very well because of your COMT/VDR taq status. The recommended procedure in this case is to use hydroxyb12 (a nonactive form of b12 that is a natural form in the body, unlike cyancobalamin) possibly with some adenosylb12 (the active form used by the mithochondria). Ive done some digging around, and found a couple people with hetero comt mutations said they are able to get away with a little bit of mb12. I also think you could get away with more if you were to simultaneously use a methyl sink such as niacin. That idea is an original creation of mine and though not necessarily proven, I have used it myself successfully and see no reason that it shouldnt work, especially if getting mb12 is a priority, as it might be in your case considering your ms like symptoms.

SHMT1 C1420T rs1979277 AG +/-

This enzyme acts in an in-between conversion of dietary folate and the final form of methylfolate that methylates cobalamin and in another reaction takes that in between product and converts it into folinic acid. This mutation is a downregulation that results in less methylfolate and folinic acid. Less methylfolate = slowed methylation. Folinic acid is used in dna construction and a lack of it shows up the most in fast turnover cell needs, particularly the lining of the gut and the immune system. Leaky gut and low immune function result. This is one of the first things to supplement, folinic acid is easy to find and the possiblity of side effects is low, though some people report a “toxic” feeling and increased brain fog.

An ACAT mutation can also result in lowered fat metabolism, lowered energy production, and even mitochondrial dysfunction. Floating (fatty) stools and bumpy skin on your arms and legs called keratosis pilaris (chicken skin) are common symptoms. You were also more likely to have cradle cap.

From Pathways on SHMT and ACAT:

First Priority Mutations Addressing SHMT and ACAT Mutations

People with the SHMT and/or ACAT mutations sometimes have a greater tendency to experience gut dysbiosis and imbalanced flora. Until the flora are balanced, there’s a risk that the undesirable microbes will retain toxic metals. So, for those with ACAT or SHMT as well as other mutations (such as the MTHFR A1298C) that confer a greater likelihood of retaining aluminum, it is essential, prior to addressing these other mutations, to first stabilize the general gut environment via SHMT and/or ACAT support, by using supplements in the MPA received with your test results.

If both SHMT+ and ACAT + are present, begin with SHMT support first, and once that is in place, layer in ACAT support. Understanding SHMT Mutations

Based on the research of Dr. Patrick Stover, I’ve concluded that the SHMT mutation often shifts the methylation cycle away from both the long and short routes through the methylation cycle into a side reaction that leads to the production of thymidine (see illustration.)

Supplementing with nucleotides, which are a form of our DNA bases, can help to both support thymidine, while maintaining appropriate methylation cycle activity. In addition, both iron and a form of folate called “5 formyl THF ” help to regulate SHMT activity. That’s why using lactoferrin (which helps to control iron levels) along with low doses of 5 formyl THF (found in the product, ActiFolate) help shift methylation activity back to the short and long routes around the cycle. Understanding ACAT Mutations

Helping to form cholesterol Assuring lipid balance and fluidity in the cell membranes, which in turns impacts neurological function Contributing to energy production via the Krebs cycle and its impact on the mitochondria, which signal cellular activity and supply cellular energy Mediating the accumulation of oxalates, which, in excess, can contribute to kidney stones and other health problems

ACAT contributes to cholesterol synthesis and membrane lipid balance. Bile acids are first synthesized from cholesterol and next conjugated to taurine. High taurine levels (often seen with ACAT) may reflect a lack of bile acids for conjugation. Since bile salts have been shown to increase ACAT activity, they may help ACAT issues. In addition, policosanol may help with membrane lipid balance and fluidity, which impacts neurological function.

The next portion of the pathway that may be impacted by ACAT is the level of acetyl CoA, which feeds into the top of the TCA cycle (also called the Krebs cycle) at 12:00. Benfotiamine, riboflavin, and pantothenic acid support the reactions between pyruvate and the TCA cycle. In addition, a low dose of alpha lipoic acid (ALA) has been shown to replace acetyl CoA in certain reactions. Either a sprinkle of the ALA supplement or the topical ALA lotion can be used. More is not always better when it comes to support with ALA, although in some cases high dose ALA has been reported to have wonderful effects. ALA use should be based on both genetics and biochemical lab data.

A block at the acetyl CoA point of the Krebs/TCA cycle can also lead to both an accumulation of oxalates and increased levels of methylmalonic acid (MMA). To keep the cycle moving, the oxalates at 11:00 must combine with acetyl CoA coming in at 12:00. Low-dose vitamin K and lactoferrin help with that activity.

Both ACAT and high MMA levels are addressed the same way, with adenosyl B12, other forms of B12, low dose vitamin E succinate, lactoferrin, a sprinkle of actifol (ActiFolate), and nucleotides. MMA may inhibit succinate CoQ reductase, which is vital for electron transport. Vitamin K (menaquinone) and CoQ 10 (ubiquinone) can serve as electron acceptors in these cases.

Since high methionine levels appear to accompany ACAT mutations, SAMe, bile salts, glutathione (GSH,) and CoQ10 all can help to support the conversion of methionine. Curcumin and quercetin help shift the transulfuration pathway toward GSH. Since too much GSH can feed back and inhibit an enzyme that shunts to glutathione, I like to support the overall pathway rather than merely adding GSH.

CBS A360A rs1801181 AG +/- The cbs mutation is an upregulation. An A360a mutation is considered to be minor, and a heterozygous mutation shouldnt really need much consideration. But, because ammonia depletes bh4 and you are going to need all the bh4 that you can make, if you are not going to directly supplement it (which you would need to be careful with due to comt/mao, im not saying dont, at all, it might benefit you, just sneak up on the doseage if you do) then it might be helpful to lower sulfur intake and/or use yucca root. Excess peroxides will lower BH4 as well. You are likely deficient in gluatathione and the main neutralizer of peroxides in the body is a form of it called glutathione peroxidase. Supplementing selenium will increase glutathione peroxidase and will also boost immune function (this is only recommended if you do not have any acute mercury problems).

Read chapter 8 of Yaskos Pathways to Recovery

I HIGHLY recommend you make an appointment with Dr. Armine, he is one of the few real specialists in the world in this category and is supposed to be very good at dealing with problems like this. I think he could help you alot, way more than most docs/nd’s/whatever.

kjones02;52330 wrote: Impossible, where can I read more about this again? A book, internet? I would like to know because I think it would be beneficial for me, since I like to take a b vitamin. However, I would like to get it in the right proportions. You have probably posted before where to find it.

Thats a WHOLE LOT of reading for that reason. If I come across a good summary I will pass it along. There are some decent youtube videos. What are you taking?

Impossible, first of all, thank you SO much for your thorough analysis. I really appreciate it. I read through it once, but am going to need to read through it a few more times to really start understanding it better. A few things you mentioned, I had read on other sites, so it was good confirmation (i.e.: starting with SHMT and ACAT first).

I am DEFINITElY going to call this Armine guy. It is overwhelming to piece all this together and figure out exactly what supplements I should be taking, so I need someone experienced to tell me. This guy looks super legit. Hopefully he’s not too expensive or booked.

In a weird way, I am sort of excited that I found this. I’ve been working SO hard to overcome this problem and nothing helps, and I’ve always known there was “something” that was stopping me from getting better. I always assumed it was the low dose of steroids I take for a medical condition, but it’s really just replacement for what my body should be doing.

I’ve also had several other “unexplained” issues that I wonder if this could help…I.e.: symptoms of MS (though all tests negative), and persistently low sex drive/orgasm problems. I wonder if it could all be related.

I’ll probably come back and ask questions once I’ve really digested, but thank you so much again!

See if theres a way you can take the steroids transdermally. Any good compounding pharmacy would be willing to work with you on that. Also, you are just as likely to have a viral or bacterial overload and heavy metals as you are to have candida, and all of those can do a number on the immune system.

hey again, impossible. I read through your message again and have 2 questions. I’m going to call that doctor tomorrow to see when I get get in with him

1. How do my mutations compare to yours and/or others you’ve seen? More significant? Similar? Less drastic? I’m just wondering. I only had a couple homozygous but several heterozygous, so I was just wondering if this really does seem like it could be “it” for me as to why I’m not improving. I’m thinking it has definitely potential, but just wondering on your take.

2. Do you think I could safely start on some supplements before I get in with that doctor? I have the feeling it’ll be a while until he can see me, though who knows. I know SHMT and ACAT should be addressed first since I’m hetero…as such, would it be dangerous for me to try that Folinic Acid and other supplements that go along with that? I think you mentioned methlyfolate (but no good for me — rather mb12??), 5 formyl THF (actifolate), adenosyl b12, other b12, etc. Does that seem like a good plan? If so, maybe just focus on the Folinic, mb12 and 5 formyl THF? What do you think?

yisucks;52350 wrote: hey again, impossible. I read through your message again and have 2 questions. I’m going to call that doctor tomorrow to see when I get get in with him

1. How do my mutations compare to yours and/or others you’ve seen? More significant? Similar? Less drastic? I’m just wondering. I only had a couple homozygous but several heterozygous, so I was just wondering if this really does seem like it could be “it” for me as to why I’m not improving. I’m thinking it has definitely potential, but just wondering on your take.

2. Do you think I could safely start on some supplements before I get in with that doctor? I have the feeling it’ll be a while until he can see me, though who knows. I know SHMT and ACAT should be addressed first since I’m hetero…as such, would it be dangerous for me to try that Folinic Acid and other supplements that go along with that? I think you mentioned methlyfolate (but no good for me — rather mb12??), 5 formyl THF (actifolate), adenosyl b12, other b12, etc. Does that seem like a good plan? If so, maybe just focus on the Folinic, mb12 and 5 formyl THF? What do you think?

Thanks so much again!

We are somewhat similar, though I dont have acat, comt, mao, or mthfr mutations and I have multiple bhmt mutations. Im a little worse off than you in regards to total methyl status. The fact that you are not using up as many methyl groups (or SAMe, however you want to look at it) breaking down neurotransmitters helps in those regards. But your b12 status is likely worse than mine with the other mutation. Mtr/ mtrr and shmt will definately slow things down. Anyone that says otherwise because a mthfr 677 mutation isnt present does not know what they are talking about. Alot of doctors will even say this, but its not right. Plus, everyone ive seen with that combo, including myself, has really responded to treatment. SHMT will directly hurt immune function too. Lowered atp production because of the acat mutation can hurt immune function too. Its all not likely to be your entire problem, as far as candida is concerned, but is definately a piece of the puzzle.

It would be safe for you to add in 200 mcg folinic acid (which is 5 formylthf, actifolate contains other forms too btw) and some hydroxyb12, start with 1 or 200 mcg sublingual. Start those one at a time to see how each makes you feel. Wait to add in the other forms of b12 until your under the care of Armine or whoever.

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